Introduction

Bell’s palsy is the diagnosis for acute onset of weakness or paralysis of all muscle groups on one side of the face that cannot be explained by local trauma, disease of the central nervous system, or other causes (e.g. stroke, brain or facial nerve cancer, or systemic infectious diseases) [1, 2]. For this reason, Bell’s palsy is also known as idiopathic facial paralysis, indicating the unknown etiology of the disorder. A proposed mechanism is compression of the facial nerve (cranial nerve VII) due to inflammation, whether caused by viral infection or ischemia (e.g. arteriolar spasm) [1]. The symptoms of this disorder are related to malfunction in the facial nerve, and include paresis, paralysis, fasciculations, drooping of the eyelid or corner of the mouth, and loss of taste sensation in the anterior tongue [2, 3]. These may lead to secondary complications, such as eye injury, impaired speech, eating difficulty, and potential depression resultant to social isolation. The disease is named after the surgeon Sir Charles Bell, who identified the disorder in 1844 [3, 4].

The incidence of Bell’s palsy increases with age, and it most commonly presents in patients from 15-45 years of age [3, 5]. The recurrence rate is approximately 10% [1]. There is no bias towards the left or right facial nerve; the diagnosis of Bell’s palsy is given as frequently to male patients as to females [6]. Bell’s palsy tends to appear more often in patients with existing herpes simplex virus (HSV). Some research has suggested a slightly higher incidence in diabetes mellitus patients due to increased fluid pressure impinging blood flow to the facial nerve; the damage possibly results from chronic ischemia [4, 7, 8]. A possible connection to pregnancy has been suggested for Bell’s palsy, with compression of the facial nerve secondary to increased fluid pressure and edema (related to pre-eclampsia) [8].

Functional Anatomical Review

Facial Musculature

The primary muscles of facial expression innervated by the facial nerve are listed below, accompanied by a brief description of their action(s) (Figure 1) [9]:
Frontalis: Elevation of the eyebrows and wrinkling of the forehead

Orbicularis oculi: Closing or narrowing the eye

Orbicularis oris: Closing and puckering the lips

Zygomaticus: Elevation of the corners of the mouth

Buccinator: Compression of the cheeks

Levator labii superioris: Elevation of upper lip

Depressor labii inferioris: Depression of lower lip

Nasalis: Opening and closing of nostrils

Platysma: Pouting of lips

Figure 1: Muscles of facial expression, anterior view.
Figure 1: Muscles of facial expression, anterior view.

Facial Nerve and Facial Nuclei: Overview

The facial nerve (cranial nerve VII) supplies efferent motor fibers to the muscles of facial expression and the stapedius muscle (located in the inner ear); secretomotor fibers to the glands of the head and neck (submandibular, sublingual, nasal, palatine, pharyngeal, and lacrimal glands); and afferent (gustatory) fibers from the anterior 2/3 of the tongue. In the caudal pons, the facial nerve arises from the facial nuclei (Figure 2), which can be divided into two functional and structural components. The upper portion of the facial nucleus receives projections from both ipsilateral and contralateral cortical fibers; it innervates the musculature of the upper face. The lower portion of the facial nucleus predominantly receives contralateral cortical input, and innervates the lower facial muscles. The course of the facial nerve is traced in Figure 3 [9, 10].

Figure 2: Cranial nerve VII leaving brain stem nuclei at pontomedullary junction.
Figure 2: Cranial nerve VII leaving brain stem nuclei at pontomedullary junction.

Figure 3: Overview of facial nerve components.
Figure 3: Overview of facial nerve components.

Neurological Pathways

Supranuclear pathways

The voluntary motor components of facial expression originate in the precentral gyrus of Brodmann’s area 4, the primary motor cortex (M1). Based on the somatotopic map of movements on the motor cortex, upper motor neurons serving the facial muscles originate laterally. Pyramidal neurons in M1 descend via the posterior limb of the internal capsule via the corticonuclear (corticobulbar) projections; neurons serving the muscles of the upper face descend, terminating bilaterally in the facial nuclei in the brainstem, while neurons serving the lower face decussate and innervate the contralateral facial nucleus [10]. As a result, the facial nuclei contain both crossed and uncrossed fibers (Figures 4, 5).

Figure 4: Comparison of pathways involved in UMN and LMN lesions affecting the face. The upper face is innervated bilaterally, while the lower face is innervated unilaterally.
Figure 4: Comparison of pathways involved in UMN and LMN lesions affecting the face. The upper face is innervated bilaterally, while the lower face is innervated unilaterally.

Figure 5: Innervation of muscles of facial expression.
Figure 5: Innervation of muscles of facial expression.

Inputs for the involuntary emotional components of facial expression originate in the basal ganglia and limbic system, which facilitate facial manifestation of emotional sensations. Other inputs influencing facial movement also arise from the visual system (controlling the blink reflex), trigeminal nucleus (corneal reflex), auditory nucleus (eye closure in response to loud noises), and autonomic centers [10].

Intracranial pathways

Four nuclei located in the caudal pons contribute to the facial nerve (cranial nerve VII): these include the motor nucleus, located in the reticular formation; the superior salivatory nucleus (parasympathetic function); the lacrimatory nucleus (parasympathetic function); and the tractus solitarius nucleus, containing special sensory (gustatory) afferents from the anterior 2/3 of the tongue [11, 12]. A motor and a sensory root arise from the lower border of the pons, travel through the internal auditory meatus and into the facial canal, located in the temporal bone. Here, the roots join into the single trunk of the facial nerve, form the geniculate ganglion, and then give rise to three intracranial branches (motor, secretomotor, and gustatory). The stylomastoid foramen serves as the exit point from the cranium for the facial nerve (Figure 6) [13].

Figure 6: Superior view of the route of cranial nerve VII from the pons through the cranium.
Figure 6: Superior view of the route of cranial nerve VII from the pons through the cranium.


Extracranial pathways

After passing through the stylomastoid foramen, the facial nerve takes a path anterior to the outer ear. Here again, three branches arise: the posterior auricular nerve, the motor fibers serving the digastric muscle, and the motor fibers serving the stylohyoid muscle. Finally, the main trunk of the facial nerves enters the parotid gland and divides into five terminal motor branches: temporal, zygomatic, buccal, marginal mandibular, and cervical (Table 1, Figure 7) [13]. A mnemonic device that may help to remember the five branches is “Two Zombies Bit My Cat.”
Terminal Motor Branches of Facial Nerve

Innervation
Temporal

Frontalis, orbicularis oculi, corrugator supercilli, & pyramidalis muscles
Zygomatic

Zygomaticus major, zytomaticus minor, elevator ala nasi, levator labii
superioris, caninus, depressor septi, compressor nasi, & dilator naris muscles
Buccal

Buccinator, & superior orbicularis oris muscles
Marginal mandibular

Risorius, quadratus labii inferioris, triangularis, mentalis, inferior orbicularis
oris muscles
Cervical

Platysma muscle
Table 1: The five terminal motor branches of the facial nerve and the muscles of facial expression they innervate [14].

Figure 7: The five terminal (motor) branches of the facial nerve include the temporal zygomatic, buccal, mandibular, and cervical branches.
Figure 7: The five terminal (motor) branches of the facial nerve include the temporal zygomatic, buccal, mandibular, and cervical branches.

Pathophysiology

Bell’s palsy has been termed “a diagnosis of exclusion” for the reason that it is idiopathic – resulting from no identifiable other cause [2, 3]. The paralysis, paresis and other symptoms are likely the product of inflammatory mechanisms affecting the conductive ability of the facial nerve; due to its passage within the narrow temporal canal, any swelling would not only lead to nerve compression but also impair circulation. It has been suggested that viral infection (e.g. Herpes zoster, mumps, rubella, vericella, infectious mononucleosis) plays a role because of the higher incidence in those with herpes infections, for example; this makes sense because viral infection can lead to inflammation as well as nerve demyelination and degeneration. However, virus isolation and antibody studies have not provided strong supporting evidence [1, 3, 4]. Other studies have suggested a purely ischemic origin linked to increased blood pressure and fluid retention, such as in diabetes mellitus, malignant hypertension, arteriolar disease, and pre-eclampsia [1, 2]. Insufficiency of circulation to the facial nerve could lead to swelling and compression; this explanation has been supported by the relative success of therapeutic steroids such as adrenocorticotropic hormone (ACTH) and prednisolone [1].

Because the facial nerve innervates muscles of facial expression, salivary and lacrimal glands, and the stapedius muscles, and conveys gustatory fibers from the anterior tongue, the symptoms of Bell’s palsy can be understood in this context (Figure 8) [3, 6, 7, 15].

  • Unilateral Paresis/paralysis – weakness or inability to contract facial musculature, leading to lack of expression, drooping of the corners of the mouth and eye on the ipsilateral side of the face.
  • Loss of taste in anterior 2/3 tongue – results from damage proximal to the chorda tympani branch, which carries taste fibers from the tongue to the central nervous system.
  • Drooling or dry mouth – either symptom can result from dysregulation of parasympathetic control on salivary glands (sublingual and submandibular) from damage proximal to the chorda tympani branch.
  • Excessive tearing or dry eyes – either symptom can result from dysregulation of parasympathetic control on lacrimal glands
  • Loss of corneal reflex – an inability to reflexively close the eye in response to corneal stimulation; results from damage to motor (efferent) fibers in the temporal and zygomatic branches of the facial nerve.
  • Facial numbness – results from damage to the parts of the facial nerve carrying general sensory afferents for pain and touch.
  • Hyperacusis – Increased sensitivity to sound, resulting from loss of innervation to the stapedius muscle. Contraction of the stapedius muscle dampens excessive vibration from sound, so loss of this function can lead to intolerance to noise and a sense of aural fullness.
Figure 8: Lower motor neuron lesion in Bell's palsy, demonstrating several common symptoms of the disorder.
Figure 8: Lower motor neuron lesion in Bell's palsy, demonstrating several common symptoms of the disorder.


Treatment and Prognosis

The majority (70–85%) of cases of Bell’s palsy demonstrate spontaneous resolution of symptoms over a recovery period of up to six months and show full recovery, while the remainder show varying degrees of paresis or even paralysis, with accompanying symptoms [4, 5, 6]. The consequences of facial nerve degeneration resulting from prolonged compression or ischemia may be permanent disability [4]. Clinical tests of denervation by stimulating the nerve percutaneously can yield predictions of recovery, with extent of denervation predicting long-term loss of function; on the other hand, early and spontaneous resolution of symptoms is generally predictive of full recovery [1].
Several treatments have been proposed, including administration of steroids, antiviral medication, physical therapy, and surgical decompression. Unless the onset of the palsy is accompanied by pain, (an occurrence which is predictive of a poor outcome,) the most recommended treatment is actually to allow the disorder to resolve on its own. To address the immediate issue of nerve inflammation and swelling, oral steroids such as adrenocorticotropic hormone (ACTH) and prednisolone are usually prescribed for adult patients within 72 hours of onset; these can be augmented by antiviral therapy if indicated by patient history or clinical circumstances [3]. For individuals who experience eye dryness, paralysis of the eyelid, or lack of corneal reflex, eye protection is recommended to prevent corneal injury. Analgesics such as ibuprofen may be given for temporary relief of pain and discomfort. Surgical decompression of the temporal canal has been attempted, but many reviewers have argued that there is no evidence from controlled studies to indicate that its usefulness outweighs the potential risks [1, 3, 5]. The effectiveness of physical therapy or acupuncture is contested, but these treatments are not broadly applied at present [3]. An important consideration for clinicians presented with unilateral facial palsy is to eliminate differential diagnoses, such as stroke, Lyme disease, and tumors of the facial nerve [5, 16].

Conclusion

Bell’s palsy, or idiopathic facial paralysis, is a disorder of unknown etiology characterized by the sudden onset of unilateral weakness or paralysis, along with associated symptoms of damage to the facial nerve. Relevant symptoms include lack of facial expression, unilateral numbness, drooping of the eyelid or corner of the mouth, hyperacusis, loss of taste sensations of the anterior tongue, and loss of adequate parasympathetic control to the salivary and lacrimal glands. The palsy typically resolves spontaneously without intervention, but the most common treatments are oral steroids, alone or in combination with antivirals. If facial nerve compression and inflammation lead to denervation, long-term disability may be a consequence. However, most individuals with Bell’s palsy return to full function within six months.

Quiz

Multiple Guess and True/False

1. The most common cause of Bell’s palsy is:
  • a. Viral infection
  • b. Malignant hypertension
  • c. Idiopathic etiology
  • d. Direct trauma
  • e. Facial nerve tumor

2. Which cranial nerve is affected in Bell's palsy?
  • a. Trigeminal (CN V)
  • b. Facial (CN VII)
  • c. Vagus (CN X)
  • d. All of the above

3. Second to allowing for spontaneous recovery from Bell’s palsy, the recommended treatment is to administer steroids within 72 hours of onset. (T/F)

4. The loss of taste experienced by Bell’s palsy patients results from a disruption in which branch of the facial nerve?
  • a. The greater superficial petrosal nerve
  • b. The chorda tympani nerve
  • c. The posterior auricular nerve
  • d. The lesser petrosal nerve

5. What are the primary function(s) of the facial nerve?
  • a. Control of blinking and eyelid closure
  • b. Control of facial expression
  • c. Innervation of lacrimal and salivary glands
  • d. (a) and (b)
  • e. All of the above

6. Symptoms of dry mouth or drooling can result from disruptions to the buccal and marginal mandibular branches of the facial nerve. (T/F)

7. Hyperacusis in Bell’s palsy is due to the paralysis of the following muscle:
  • a. Tensor tympani
  • b. Levator veli palatine
  • c. Tensor veli palatine
  • d. Stapedius

8. Individuals with Bell's palsy can typically contract the musculature needed to wrinkle the forehead. (T/F)

9. What are common treatments for Bell's palsy?
  • a. Steroids
  • b. Antivirals
  • c. Analgesics
  • d. All of the above

10. Bell's palsy has a hereditary component. (T/F)

11. Bell's palsy preferentially affects the right side of the face. (T/F)

Short Answer

12. Describe the proposed mechanisms by which viral infection or ischemia might trigger Bell’s palsy.

13. Given the areas innervated by the facial nerve, how might Bell’s palsy cause difficulty in swallowing? Include in your answer which branch of the facial nerve would be responsible and the musculature involved.

14. What is a possible explanation for a higher incidence of Bell’s palsy in pregnant women and chronic hypertensive patients?

15. Patients with apparent Bell’s palsy are often tested for diabetes mellitus and Lyme disease. Why might these tests be appropriate?

Answer Key

1. (c); 2. (b); 3. T; 4. (b); 5. (e); 6. F; 7. (d); 8. F; 9. (d); 10. F; 11. F; 12-15 open response.

Glossary

  • Afferent – Relating to information from the periphery that travels toward the central nervous system (often sensory in nature).
  • Contralateral – Relating to the opposite side of the body as the point of reference.
  • Afferent – Relating to information from the central nervous system that travels toward the periphery (often motor in nature).
  • Idiopathic – A description of a disease or disorder with unknown etiology, such as Bell’s palsy.
  • Ipsilateral – Relating to the same side of the body as the point of reference (e.g. Bell’s palsy results in paresis to the side of the face as the damaged facial nerve).
  • Ischemia – Lack of sufficient blood supply to an organ or body part, often resulting in damage to that structure.
  • Paralysis – Complete loss of ability to contract muscles or generate movement.
  • Paresis – Weakness or partial loss in ability to contract muscles.
  • Unilateral – On one side of the body.

Suggested further reading


Acknowledgements

Many thanks to the Department of Kinesiology at Gordon College and to Dr. Sean Clark, Ph.D., for his instruction in this neurophysiology class.

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